{"classes":[{"categories":[{"measurements":[{"groupId":"OG000","lowerLimit":"62.4","upperLimit":"89.4","value":"78.0"},{"groupId":"OG001","lowerLimit":"72.1","upperLimit":"94.7","value":"86.0"}]}],"denoms":[{"counts":[{"groupId":"OG000","value":"41"},{"groupId":"OG001","value":"43"}],"units":"Participants"}],"title":"M918T"},{"categories":[{"measurements":[{"groupId":"OG000","lowerLimit":"46.2","upperLimit":"95.0","value":"76.9"},{"groupId":"OG001","lowerLimit":"79.6","upperLimit":"99.9","value":"96.0"}]}],"denoms":[{"counts":[{"groupId":"OG000","value":"13"},{"groupId":"OG001","value":"25"}],"units":"Participants"}],"title":"Cysteine Rich Domain"},{"categories":[{"measurements":[{"groupId":"OG000","lowerLimit":"15.8","upperLimit":"100","value":"100"},{"groupId":"OG001","lowerLimit":"2.5","upperLimit":"100","value":"100"}]}],"denoms":[{"counts":[{"groupId":"OG000","value":"2"},{"groupId":"OG001","value":"1"}],"units":"Participants"}],"title":"V804X"},{"categories":[{"measurements":[{"groupId":"OG000","lowerLimit":"39.8","upperLimit":"100","value":"100"},{"groupId":"OG001","lowerLimit":"29.2","upperLimit":"100","value":"100"}]}],"denoms":[{"counts":[{"groupId":"OG000","value":"4"},{"groupId":"OG001","value":"3"}],"units":"Participants"}],"title":"Other"}],"denoms":[{"counts":[{"groupId":"OG000","value":"60"},{"groupId":"OG001","value":"72"}],"units":"Participants"}],"description":"Oncogenic RET activation has been implicated as a driver in MTC. These rearrangements typically produce chimeric transcripts that encode a fusion protein consisting of the RET kinase domain coupled to a protein with a dimerization domain (e.g., M918T, cysteine rich domain, V804X). RET genotypes were determined by local testing and/or central analysis of ctDNA. CBR was assessed in participants having specific RET rearrangements. CBR was defined as the percentage of participants with a confirmed CR or PR, or SD which has been lasting at least 16 weeks (i.e. 4 cycles if 28 days are in one cycle) from the first dose date. CR and PR were defined per RECIST as outlined in the description for OM 3. SD was defined as neither sufficient shrinkage to qualify for CR or PR nor sufficient increase to qualify for PD. PD was defined as at least a 20% increase in SOD of target lesions, taking as reference the smallest SOD on study (including baseline).","dispersionType":"95% Confidence Interval","groups":[{"description":"Participants who had RET- mutation positive MTC previously treated with either cabozantinib and/or vandetanib therapies received pralsetinib, 400 mg orally, QD until discontinuation due to toxicity, disease progression, or other reasons.","id":"OG000","title":"RET-mutation MTC With Prior Cabozantinib and/or Vandetanib Treatment"},{"description":"Participants who had RET- mutation positive MTC not previously treated with cabozantinib or vandetanib therapies received pralsetinib, 400 mg orally, QD until discontinuation due to toxicity, disease progression, or other reasons.","id":"OG001","title":"RET-mutation MTC With No Prior Cabozantinib or Vandetanib Treatment"}],"paramType":"NUMBER","populationDescription":"RET-altered measurable disease population included participants in the efficacy population who have measurable (target) disease per RECIST v1.1, at baseline according to BICR and sufficient evidence of a RET alteration. As prespecified in the SAP, Phase 1 participants treated at 400 mg QD are pooled with Phase 2 participants for efficacy analysis. Number analyzed is the number of participants with the specified mutation.","reportingStatus":"POSTED","timeFrame":"Up to approximately 79.8 months","title":"Phase 1 and Phase 2: CBR in RET-mutation MTC Participants With Specific RET Gene Status","type":"SECONDARY","unitOfMeasure":"percentage of participants"}